Article

Coenzyme Q10: an independent predictor of mortality in chronic heart failure.

Clinical Biochemistry Unit, Canterbury Health Laboratories, Christchurch, New Zealand.
Journal of the American College of Cardiology (Impact Factor: 14.09). 11/2008; 52(18):1435-41. DOI: 10.1016/j.jacc.2008.07.044
Source: PubMed

ABSTRACT The aim of this study was to investigate the relationship between plasma coenzyme Q(10) (CoQ(10)) and survival in patients with chronic heart failure (CHF).
Patients with CHF have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. Therefore we tested the hypothesis that plasma CoQ(10) is a predictor of total mortality in CHF and could explain this association.
Plasma samples from 236 patients admitted to the hospital with CHF, with a median (range) duration of follow-up of 2.69 (0.12 to 5.75) years, were assayed for LDL-C, TC, and total CoQ(10).
Median age at admission was 77 years. Median (range) CoQ(10) concentration was 0.68 (0.18 to 1.75) micromol/l. The optimal CoQ(10) concentration for prediction of mortality (established with receiver-operator characteristic [ROC] curves) was 0.73 micromol/l. Multivariable analysis allowing for effects of standard predictors of survival--including age at admission, gender, previous myocardial infarction, N-terminal peptide of B-type natriuretic peptide, and estimated glomerular filtration rate (modification of diet in renal disease)--indicated CoQ(10) was an independent predictor of survival, whether dichotomized at the ROC curve cut-point (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.2 to 3.3) or the median (HR: 1.6; 95% CI: 1.0 to 2.6).
Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).

0 Bookmarks
 · 
140 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cardiovascular disease is the primary cause of morbidity and mortality amongst the diabetic population. Both experimental and clinical evidence suggest that diabetic subjects are predisposed to a distinct cardiomyopathy, independent of concomitant macro- and microvascular disorders. 'Diabetic cardiomyopathy' is characterized by early impairments in diastolic function, accompanied by the development of cardiomyocyte hypertrophy, myocardial fibrosis and cardiomyocyte apoptosis. The pathophysiology underlying diabetes-induced cardiac damage is complex and multifactorial, with elevated oxidative stress a key contributor. We now review the current evidence of molecular disturbances present in the diabetic heart, and their role in the development of diabetes-induced impairments in myocardial function and structure. Our focus incorporates both the contribution of increased reactive oxygen species production and reduced antioxidant defenses to diabetic cardiomyopathy, together with modulation of protein signaling pathways and the emerging role of protein O-GlcNAcylation and miRNA dysregulation in the progression of diabetic heart disease. Lastly, we discuss both conventional and novel therapeutic approaches for the treatment of left ventricular dysfunction in diabetic patients, from inhibition of the renin-angiotensin-aldosterone-system, through recent evidence favoring supplementation of endogenous antioxidants for the treatment of diabetic cardiomyopathy. Novel therapeutic strategies, such as gene therapy targeting the phosphoinositide 3-kinase PI3K(p110α) signaling pathway, and miRNA dysregulation, are also reviewed. Targeting redox stress and protective protein signaling pathways may represent a future strategy for combating the ever-increasing incidence of heart failure in the diabetic population.
    Pharmacology [?] Therapeutics 01/2014; · 7.79 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Coenzyme Q₁₀ (Co Q₁₀) or ubiquinone was known for its key role in mitochondrial bioenergetics as electron and proton carrier; later studies demonstrated its presence in other cellular membranes and in blood plasma, and extensively investigated its antioxidant role. These two functions constitute the basis for supporting the clinical indication of Co Q₁₀. Furthermore, recent data indicate that Co Q₁₀ affects expression of genes involved in human cell signalling, metabolism and transport and some of the effects of Co Q₁₀ supplementation may be due to this property. Co Q₁₀ deficiencies are due to autosomal recessive mutations, mitochondrial diseases, ageing-related oxidative stress and carcinogenesis processes, and also a secondary effect of statin treatment. Many neurodegenerative disorders, diabetes, cancer, fibromyalgia, muscular and cardiovascular diseases have been associated with low Co Q₁₀ levels. Co Q₁₀ treatment does not cause serious adverse effects in humans and new formulations have been developed that increase Co Q₁₀ absorption and tissue distribution. Oral Co Q₁₀ treatment is a frequent mitochondrial energizer and antioxidant strategy in many diseases that may provide a significant symptomatic benefit.
    Frontiers in Bioscience 01/2014; 19:619-33. · 3.29 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The impact of aging and physical capacity on coenzyme Q10 (Q10) levels in human blood is unknown. Plasma Q10 is an important factor in cardiovascular diseases. To understand how physical activity in the elderly affects endogenous Q10 levels in blood plasma, we studied a cohort of healthy community-dwelling people. Volunteers were subjected to different tests of the Functional Fitness Test Battery including handgrip strength, six-minute walk, 30 seconds chair to stand, and time up and go tests. Anthropometric characteristics, plasma Q10 and lipid peroxidation (MDA) levels were determined. Population was divided according to gender and fitness. We found that people showing higher levels of functional capacity presented lower levels of cholesterol and lipid peroxidation accompanied by higher levels of Q10 in plasma. The ratio Q10/cholesterol and Q10/LDL increased in these people. No relationship was found when correlated to muscle strength or agility. On the other hand, obesity was related to lower Q10 and higher MDA levels in plasma affecting women more significantly. Our data demonstrate for the first time that physical activity at advanced age can increase the levels of Q10 and lower the levels of lipid peroxidation in plasma, probably reducing the progression of cardiovascular diseases.
    Experimental gerontology 01/2014; · 3.34 Impact Factor

Full-text (2 Sources)

View
32 Downloads
Available from
May 24, 2014